New Research

Jan. 27, 2018

Research Paper of the Month

We highlight this paper first because one of our board members, Dr. Robert Paine, was one of the authors and the study was done here on the Wasatch Front. Investigators from the University of Utah and Intermountain Medical Center found that the risk of pneumonia and the severity of the illness (including ICU admission and need for critical care) was increased in response to a few days of increased PM2.5 levels. Like with so many other studies, these effects were seen even at levels below EPA standards.

More research showing the relationship between air pollution and adverse birth outcomes. In the case of the study below, an analysis of over 1.3 million births in China showed not only higher rates of pre-term births with more air pollution, but the correlation was stronger the more premature the birth.

Shutting down a coal power plant was followed by an increase in birth weight of newborns downwind from the plant.

Yang M, et al. The Impact of Environmental Regulation on Fetal Health: Evidence from the Shutdown of a Coal-Fired Power Plant Located Upwind of New Jersey. Journal of Environmental Economics and Management, 2017; DOI: 10.1016/j.jeem.2017.11.005

More evidence of air pollution contributes to metabolic disorders, i.e. type II diabetes, insulin resistance, and interferes with glucose metabolism.

Air pollution is associated with higher risk for developing and seeking treatment for mental disorders, and a much higher mortality risk for those with mental health and behavioral disorders, including suicide.

This study showed that a biological pathway for air pollution’s involvement in strokes and heart attacks is the release of inflammatory chemicals that alter the functioning of genes involved in the regulation of blood vessels.

This study in mice shows that an anti-oxidant in grapefruit, reduces the DNA damage and oxidative stress in heart cells, and the tendency for blood clot formation caused by diesel exhaust. This is just one study, but there’s no down side to eating more grapefruit.

Multiple studies have shown air pollution affects male sperm. The studies below add to that data base, including one that shows it reduces the y/x chromosome ratio in sperm which would result in a decrease in percentage of male newborns compared to females.

Hundreds of studies have shown increased overall mortality from air pollution, most of that is assumed to occur in the vulnerable subsets of the adult population, especially the elderly. Far fewer studies have been done exploring possible increased rates of infant mortality. The study below adds significantly to the evidence that air pollution also contributes to infant mortality. Almost 500,000 infants were tracked for over 6 years. Researchers found a very strong association between small increases in PM2.5 and total infant deaths, respiratory deaths, and SIDS. Specifically 1.3 ug/m3 increases in PM2.5 increased the rate of these outcomes between 200% and 300%.

Acceleration of the aging process is part of the clinical consequence of air pollution exposure. Telomere length is a marker of biological aging. This study showed that prenatal air pollution provokes shorter telomere length in the newborns, measured in the umbilical cord and placenta.

In this rather elaborate study, the heart and lung benefits of exercise walking were offset by air pollution inhaled along a busy road.

Sinharay R, et al. Respiratory and cardiovascular responses to walking down a traffic-polluted road compared with walking in a traffic-free area in participants aged 60 years and older with chronic lung or heart disease and age-matched healthy controls: a randomised, crosso. The Lancet, 2017; DOI:

We have stated previously that air pollution harms all major organ systems. The evidence for an affect on kidneys has been sparse however. This new study shows evidence that air pollution has a significant association with impaired kidney function.

Another study showing that air pollution impairs cognitive abilities of children. In particular these studies measured the amount of air pollution that children breathed on the way to school, which correlated with decreased memory.

Forns J, et al. Longitudinal association between air pollution exposure at school and cognitive development in school children over a period of 3.5 years. Environ Res. 2017 Aug 28;159:416-421. doi: 10.1016/j.envres.2017.08.031. [Epub ahead of print]

Benzene, SO2, and NOx were associated with increased rates of lung and bladder cancer, primarily in women over the age of 75.

Collarile P, et al. Residence in Proximity of a Coal-Oil-Fired Thermal Power Plant and Risk of Lung and Bladder Cancer in North-Eastern Italy. A Population-Based Study: 1995-2009.

In utero exposure to air pollution, specifically diesel exhaust, has been shown in animals to lead to heart failure in adulthood. This study showed that a likely mechanism is the alteration of genes that play a role in the the functioning of heart cells.

This study shows that in healthy college age students, higher air pollution led to significant increases in stress hormones–cortisol, cortisone, epinephrine, and norepinephrine, higher blood pressure, insulin resistance, and biomarkers of oxidative stress and inflammation

More evidence that air pollution shortens life expectancy and causes premature death.

Ebenstein A, et al. New evidence on the impact of sustained exposure to air pollution on life expectancy from China’s Huai River Policy. Proceedings of the National Academy of Sciences, 2017; 201616784 DOI: 10.1073/pnas.1616784114

Both chronic and acute ozone exposure during pregnancy increase the risk of still birth, as much as 39% even at levels below the EPA’s standards. Even the ozone levels in the week prior to delivery increase the risk. About 8,000 still births a year occur nationally due to ozone. Extrapolating from that research to Utah indicates about 100 still births a year occur in Utah due to our ozone, and that doesn’t count the risk of PM2.5.

Even air pollution levels slightly above background levels are associated withe increased rates of hospitalization for all causes, and for respiratory and heart problems in particular. Like other studies on mortality, the rate of increase per unit of exposure, was even greater at PM 2.5 levels below 8 ug/m3. The current annual EPA standard is 12. Background levels of PM2.5 are about 5 ug/m3.

This is a landmark study on air pollution and mortality, involving 61 million people from throughout the country. It is published in the most prestigious journal in the world, the New England Journal of Medicine. It significantly strengthens the association between premature death and PM2.5 and ozone. The key findings were that levels of both pollutants, well below the EPA’s standards are still strongly associated with mortality. Specifically, for every 10 ug/m3 of chronic PM2.5 exposure mortality in 7.3%, or .73% for every 1 ug/m3. For ozone, for every 10 ppb, the mortality increased 1.1%. However, at lower concentrations, that association was even stronger. For those people exposed to levels of PM2.5 below 12 ug/m3 (the current EPA annual standard), and below 50 ppb ozone (the current EPA standard is 70 ppb), the risk of death increased to 1.36% for every 1 ug/m3 for PM2.5, and continued at the same rate for ozone, i.e. 1% for every 10 ppb.

This is the strongest research statement yet to establish that: 1. There is no safe level of air pollution. 2. Current EPA standards are inadequate and out of step with the science. 3. The health hazard per unit off exposure is actually greater at the lowest doses. That means public policy needs to address the problem even for those cities that have relatively clean air. 4. The current administration’s attempt to delay or role back standards will do even more harm than what has been previously calculated.

The subjects in this study below were children, teenagers, and young adults in Mexico City where the particulate pollution is still quite high, despite many public policy changes to address it. This is the second study to show that these tiny pollution nanoparticles from fossil fuel combustion end up inside our brains. Once there they can cause brain damage, disrupting cellular and intracellular architecture. This undoubtedly contributes to the many clinical studies that show impaired brain function, loss of memory, loss of intellectual abilities, behavior problems, and more degenerative brain diseases in people exposed to more air pollution.

We should be just as concerned about the air our children breathe as we are about lead in the water they drink.

Numerous studies are showing a strong connection between pollution and type II diabetes. This study of newborns showed an increase in insulin levels, measured from cord blood, with more particulate pollution exposure. Specifically, for every 2.4 ug/m3 increase in PM2.5, insulin levels increased 13%. This suggests that pollution in utero can set the stage for type II diabetes later in life.

This paper gives us new insight into how particulate pollution causes vascular dysfunction, leading to such things heart attacks and strokes. Inhaled nanoparticles were found to accumulate in the lining of blood vessels at sites of existing inflammation and atherosclerosis, aggravating that disease process. The particles appeared in the blood and urine of human subjects within as little as 15 minutes, and were still present three months later.

Telomeres are repeating sequences of DNA at the ends of chromosomes that keep the chromosomes from unraveling. Every time the cell divides it loses some telomere length. Telomere length is closely associated with longevity. Previous studies have shown air pollution is associated with shorter placental and fetal telomere length. This study shows that in children and adolescents, air pollution exposure is associated with reduced telomere length, and that means reduced life expectancy.

Lee E, et al. Traffic-Related Air Pollution and Telomere Length in Children and Adolescents Living in Fresno, CA. Journal of Occupational and Environmental Medicine, 2017; 59 (5): 446 DOI: 10.1097/JOM.0000000000000996

As the connection between air pollution and neurodegenerative diseases steadily grows, this is one we didn’t anticipate–air pollution aggravating symptoms of Parkinson’s disease.

Air pollution accelerates brain aging, increases the deposition of amyloid beta particles in the brain, and can almost double the risk of Alzheimer’s in elderly women. Put another way, air pollution appears to be responsible for 20% of Alzheimer’s. A critical Alzheimer risk gene, magnifies the risk further, especially in women, and interacts with air pollution to accelerate brain aging.

This study suggests that the real culprit in particulate air pollution’s adverse effect on pregnancy outcomes is PAHs which are often attached to air pollution particles, rather than the particles themselves. More evidence that not all air pollution is created equal, and we should be paying much more attention to those sources that create high levels of PAH pollution–wood smoke, and industrial pollution.

The most toxic type of particulate pollution is the ultrafine category, i.e. less than 0.1 micron is size. Ultrafine pollution exposure is associated with accelerated atherosclerosis and increased rates of inflammatory bowel disease. This study reveals a likely mechanism. Ultrafines can be inhaled or ingested. This study shows that ingested ultrafine pollution altered the microbial make up of the bowel, and increased atherogenic lipid metabolites.

The closer you live to a major traffic corridor, the greater your chance of developing dementia. More evidence of the neurotoxicity of air pollution.

Chen H, et al. Living near major roads and the incidence of dementia, Parkinson’s disease, and multiple sclerosis: a population-based cohort study. Published: 04 January 2017 DOI: http://dx.doi.org/10.1016/S0140-6736(16)32399-6

The 9/11 dust cloud from the collapse of the Twin Towers in 2001, was shown to be associated with significantly higher rates of premature birth and low birth wt in the babies of pregnant women in Manhattan, nearest the site. The study’s authors stated, “the impacts are especially pronounced for fetuses exposed in the first trimester, and for male fetuses. We estimate that in this group, exposure to the dust cloud more than doubled the probability of premature delivery and had similarly large effects on the probability of low birth weight.” This is more evidence that even short term air pollution exposure can affect the developing fetus, and therefore life long health.

Changes in mitochondrial DNA (mtDNA) can serve as a marker of cumulative oxidative stress. Increased PM2.5 during the third trimester of pregnancy was associated with decreased mtDNA content suggesting heightened sensitivity to this kind biological damage in a fetus.

UPHE is adamantly opposed to the proposed project to dam the Bear River, reducing the flow to the Great Salt Lake, shrinking the lake, exposing thousands more acres of dry beach, and increasing the severity of dust storms. This study shows that dust storms in North America, like other forms of air pollution, increase mortality within a matter of days.

Air pollution’s association with cognitive decline is now well established. This study shows that among older people who also experience socioeconomic stress and disadvantage, that association is even stronger.

This study shows that for the signature outcome of air pollution exposure, a heart attack, the event is likely to be more immediate in older age groups, and more delayed in younger patients. Nonetheless, younger patients are still sensitive to the cardiovascular effects of air pollution.

Air pollution has been classified as a “Class I carcinogen” by the World Health Organization. There has been a steady increase in the incidence of Acute Myeloid Leukemia (AML) over the past several decades, and other research implicates air pollution as a trigger for leukemia. This study showed that compared to healthy children, those who had AML had significantly higher levels of “particulate matter derived nanoparticles” aggregated with blood components. This demonstrates a plausible mechanism by which air pollution could trigger AML.

This study shows that a 2.1 ug/m3 increase in chronic PM2.5 exposure was associated with a decrease in kidney function equivalent to what would be expected from 2 yrs of aging. Bear in mind that the Wasatch Front averages a PM2.5 of about 10. So that would be a decrease in kidney function equivalent to ten years of aging.

More evidence that episodic air pollution, typical of Utah’s inversions, provokes damage to the lining of blood vessels, which can contribute to acceleration of age related vascular disease, and ultimately strokes, heart attacks, sudden death, and poor pregnancy outcomes. The subjects studied were young healthy adults.

This study documents that toxic, nano-sized particles called “magnetites” found in air pollution end up in our brains. People with higher concentrations of the metallic nanoparticles are known to be at higher risk for Alzheimer’s, and the kind of brain damage these “magnetites” can cause are consistent with the disease.
At 150 nanometers or less in diameter, these particles, including iron oxide, platinum, nickel, and cobalt, whose origin can be industrial, vehicle or other sources of pollution, are small enough to be inhaled through the nose and enter the brain through the olfactory nerve system. The researchers found millions of these particles per gram of brain tissue after studying numerous autopsies. The lead study author said these results are “dreadfully shocking”.

This study showed that the Great London Smog event of 1952, was still impacting people’s health 60 years later. Those who were infants or babies in utero when they were exposed to the event (which only lasted 5 days), showed higher rates of respiratory disease measured several decades later.

Bharadwaj P, et al. Early Life Exposure to the Great Smog of 1952 and the Development of Asthma. Am J Respir Crit Care Med. First published online 08 Jul 2016 as DOI: 10.1164/rccm.201603-0451OC

We have know for several years that even low levels of particulate pollution (PM2.5) are associated with increased rates of daily death. Here is more evidence.

Air pollution accelerates the aging process, at least in part by shortening the length of telomeres. Life expectancy is proportional to telomere length, and the initial length of telomeres at birth is largely the result of environmental factors. Telomeres can be considered the cellular memories of exposure to oxidative stress and inflammation throughout a life time.

Vanadium is a heavy metal that has been recently recognized as a significant toxin, and is emitted as a byproduct of fossil fuel combustion, especially common in refinery emissions. The more vanadium in a mother’s body, the higher the rate of low birthweight

Kawasaki Disease is an inflammation of the blood vessels that afflicted infants an young children. This study showed a statistical association between KD and ozone exposure. Air pollution certainly causes inflammation, so this is not a surprise.

This is probably the best study to date showing that air pollution does indeed increase risk for still births. This meta-analysis showed a 2% increase for every 4 ug/m3 PM2.5. During a bad winter inversion and the height of the Uinta Basin drilling activity, at the one poorly placed monitor in Vernal, there was often PM2.5 of over 60. If that monitor had been placed in downtown Vernal, it would very likely have been much worse. Winter inversions in the Salt Lake Valley can reach PM2.5 levels of over 90. NOx, SO2, CO, and ozone were also shown to significantly correlate with still births. Vernal has had the unique distinction of simultaneously high ozone, and high PM2.5.

The study below showed that the multi-faceted operations of the Canadian Tar Sands are a major source of air pollution in North America. The authors state this has implications for other sources of “heavy oil” extraction. That would include the heavy black wax crude in the Uinta Basin. These two studies certainly reinforce our concern about air pollution as the most likely explanation for the spike in infant deaths in Vernal.

This is a landmark study showing chronic PM 2.5 levels of as little as 5 ug/m3 correlate with a 20% increase in development of coronary artery calcification over ten years. The EPA’s annual standard is 12.5 ug. So based on the metric from this study, what the EPA considers “safe” or acceptable, will increase the “hardening” of your arteries over 70 yrs, by 360%. Doesn’t sound very safe does it?

Kaufman, J, et al. Association between air pollution and coronary artery calcification within six metropolitan areas in the USA (the Multi-Ethnic Study of Atherosclerosis and Air Pollution): a longitudinal cohort study. DOI: http://dx.doi.org/10.1016/S0140-6736(16)00378-0

The risk of a ischemic stroke with air pollution is well established. This study shows that particulate pollution and ozone are significantly correlated with hemorrhagic stroke as well.

Following almost 67,000 people, researchers found there is a strong correlation between chronic exposure to particulate pollution, and death due to all types of cancer. In particular for every 10 ug/m3 of PM2.5 (which is about the annual average for the Wasatch Front), there was an overall increase of 22% in death from cancer, and even higher rates for lung and digestive system cancers, and an extraordinary increase of 80% in death rates for breast cancer, the most common cancer in women. Any of your loved ones have breast cancer? This should make the issue of air quality very personal to everyone.

This will likely be considered a landmark study. It shows that even air quality we label
“good,” or “green”, i.e. PM2.5 of about 10 ug/m3, doubles the incidence of “intrauterine inflammation” which is a strong predisposition for premature birth. Furthermore, it shows that level of pollution even in the first three months prior to conception, increases the risk of intrauterine inflammation 52%.

UPHE has been beating the drum on all the medical research showing how toxic air pollution is to the brain. Here is yet another study showing impairment of cognitive abilities and memory in eight year old school children.

Measuring PAH (polycyclic aromatic hydrocarbons)/DNA adducts from umbilical cord blood (as an indication of air pollution exposure), there was a significant correlation between prenatal air pollution exposure and anxiety, depression, aggressive behavior, and attention problems in children up to 11 years old.

Acrolein, one of the most toxic components in wood smoke, causes deterioration of heart muscle function after 3 hr exposure. Deterioration persisted at least as long as 24 hrs. This study done in mice.

The evidence for air pollution’s neurotoxicity continues to mount. For every 3 ug/m3 increase in NO2, considered a marker of traffic pollution, rates of Parkinson’s Disease increased 9%. Wasatch Front averages around 25 ug/m3. This study suggests that Wasatch Front pollution is associated with an increase in Parkinson’s of 72%.

The evidence on how air pollution damages the brain continues to mount. This study followed almost 100,000 people’s chronic air pollution exposure, and found an extraordinary 211% risk of Alzheimer’s per increase of 10.91 ppb in O3, a 138% risk of increase of AD per increase of 4.34 μg/m3 in PM2.5. Ozone can reach 70-80 ppb in the summer, and PM2.5 70-90 ug/m3 in the winter.

The body of research revealing the neurotoxicity of air pollution, especially polycyclic aromatic hydrocarbons (PAHs) continues to grow. This study in people over 60 yrs. old, showed this correlation between metabolites of PAHs measured in urine and cognitive testing: a 1% increase in PAHs resulted in approximately a 1.8% poorer performance.

Best EA, Juarez-Colunga E, James K, LeBlanc WG, Serdar B (2016) Biomarkers of Exposure to Polycyclic Aromatic Hydrocarbons and Cognitive Function among Elderly in the United States (National Health and Nutrition Examination Survey: 2001-2002). PLoS ONE 11(2): e0147632. doi:10.1371/journal.pone.0147632

There is a growing body of research showing a significant connection between air pollution and Type II diabetes, i.e. decreased glucose tolerance, and insulin sensitivity. This study showed short term air pollution has these effects as well as increasing bad cholesterol (LDL) , and decreasing the good cholesterol (HDL).

A 32 study meta-analysis showing significant association between PM2.5 exposure during the second and third trimesters and lower overall birth weights, and higher rates of babies who qualify as having Low Birth Weight Syndrome. Heavy metals and PAHs likely increase the toxicity of PM2.5 in causing this outcome. The authors state, “These robust results further reveal the toxic effect of PM2.5 exposure during pregnancy on fetal growth. Air pollution is ubiquitous. All pregnant women are exposed to it at some level, and immature fetuses are more susceptible.”

Even more evidence that air pollution reduces the birth weight of infants. Babies born in Beijing, China during 2008 when significant reductions in pollution were achieved for the Olympics, babies born were larger than those born in the year before and the year after.

Numerous studies have shown that air pollution is significantly correlated with rates of Type II diabetes. This study shows the possible biologic mechanism–increased levels of circulating stress hormones and lipid metabolites with even brief exposure to high levels of ozone.

Air pollution exposure during fetal development and infancy can have life long consequences. This study showed decreased lung function measured at age 16 for those adolescents that were exposed to more air pollution during the first year of life. Additional pollution exposure after that, caused further reductions in lung function.

Chronic exposure to PM2.5 is associated with loss of brain white matter in elderly women. For every 3.49 ug/m3 PM2.5 annual average, the loss of white matter was about what would be seen from 1-2 years of aging. With Salt Lake City averaging about 10 ug/m3, that means there is an acceleration of brain aging of 3-6 yrs.

This MIT study is from 2013, and we don’t know how we missed this at the time, but it certainly ramps up the relationship between pollution and mortality. Epidemiologic evidence indicates that annually, 210,000 people in the US die prematurely due to particulate pollution and ozone. And the average premature death represents a loss of life of ten years!

PM2.5 generated from coal and diesel combustion are much more potent triggers of cardiovascular disease than PM2.5 from other sources.

The bulk of the evidence suggests that people benefit from exercise, even during pollution situations. But what is the threshold at which someone does themselves more harm than good is not known. Aerobic exercise augments the overall inhaled air pollution dose, potentiates the diffusion of pollutants into circulating blood, augments oxidative stress and inflammation, raises blood pressure, impairs vascular function, and unfavorably affect autonomic balance.

Pregnant mothers who live closest to fracking sites were 40% more likely to give birth prematurely than those who live farthest away. Premature birth predisposes a baby to a lifelong increase in vulnerability to a wide variety of poor health outcomes.

Pregnant mothers more exposed to neurotoxins in air pollution, in this case styrene and chromium are more likely to give birth to children who are later diagnosed with autism. It is unclear, however, whether these chemicals are risk factors themselves or if they are just a reflection of the effect of a much larger mixture of toxic compounds.

Talbott EO, et al. Air toxics and the risk of autism spectrum disorder: the results of a population based case-control study in southwestern Pennsylvania. Environ Health. 2015 Oct 6;14:80. doi: 10.1186/s12940-015-0064-1.

May 21, 2015

Another study showing significantly increased risk for Autism Spectrum Disorder with prenatal, and post natal (up to two years after birth) exposure to PM2.5.

This paper followed 10 million people, and measured the time to first admission for any of three neurodegenerative diseases–dementia, Alzheimer’s, or Parkinson’s. They found an 8-15% increase in diagnosis of these disorders per 1 ug/m3 increase in long PM2.5 exposure. That’s a remarkably strong correlation.

Interesting paper that showed decreased birth weight and smaller head circumference in babies born to white, British mothers exposed to more PM2.5, but not in Pakistani mothers. In contrast, more PM2.5 exposure increased adiposity of newborns in Pakistani mothers, but not in white British mothers. Not sure what to make of those findings.

In Beijing China, for about one month prior to the 2008 Olympics, many of their coal fired power plants were shut down, and traffic was forcibly reduced about 50%, all in an effort to reduce pollution. In a study of 84,000 births, mothers in their 8th month of pregnancy in 2008, compared to 2007 and 2009, gave birth to babies about 1% larger. This then is yet another study showing that air pollution reduces birth weight. 1% doesn’t sound like much per baby, but it becomes a very large public health issue when thousands of babies are affected that way. Reduced birth weight is associated with an increased risk of numerous lifelong chronic diseases and impaired organ function.

More and more studies are showing how toxic air pollution is to the brain. Previous studies have shown loss of white matter volume in children exposed to air pollution in the womb, and in animals exposed shortly after birth. The study below, examining adults 60 yrs old and older, shows a loss of total brain volume (an indicator of dementia and brain atrophy) with even small increments of PM2.5. For every 2 ug/m3 increase in PM2.5, brain volume decreased 0.32% and the odds of covert brain infarcts (mini-strokes) increased 46%. Given that the EPA has recently lowered the annual PM2.5 standard to 12 ug/m3, that means air quality can meet the national standard, and still be responsible for a 2% decrease in your brain matter, and a 280% increased likelihood of provoking mini-strokes.

Yet another study showing prenatal air pollution exposure is associated with significantly worse neuropsychological development in children. For every 1 ug/m3 increase in PM2.5, motor scores were decreased 1.14 points, and every 1 ug/m3 increase in NO2 was associated with a 0.29 point decrease in mental scores. The Wasatch Front averages 38-57 ug/m3 for NO2.

Pregnant mothers exposed to air pollution demonstrate shortened placental telomeres. Placental telomeres correlate with newborn’s telomeres and telomeres are highly predictive of life expectancy. There is wide variability in the length of newborn’s telomeres, and most of that variability is related to environmental exposures. Bottom line–Maternal exposure to air pollution programs her baby to a shorter life span.

Prenatal exposure to PAH air pollutants (in high concentrations in refinery emissions, cigarette smoke and wood smoke) damages fetal brain development, shrinking the volume of white matter primarily in the left hemisphere measured in early childhood, resulting in impaired cognition, ADHD and hyperactive behavior.

Peterson B, et al. Effects of Prenatal Exposure to Air Pollutants (Polycyclic Aromatic Hydrocarbons) on the Development of Brain White Matter, Cognition, and Behavior in Later Childhood. JAMA Psychiatry. Published online March 25, 2015.doi:10.1001/jamapsychiatry.2015.57

Previous studies have shown higher rates of virtually every type of adverse pregnancy outcome with air pollution. This study of 410, 000 pregnant women showed even higher rates of gestational diabetes with air pollution–20% increase for every 5 ug/m3 of PM2.5 and 18% increase for every 5 ppb of ozone.

Large meta-analysis of 94 studies showed even short term spikes in ozone, carbon monoxide, SO2, NOx, and PM2.5 are associated with significant increases in rates of strokes. The greatest association was for the same day of exposure, although PM2.5 showed a lingering affect.

Shah A, et al. Short term exposure to air pollution and stroke: systematic review and meta-analysis. BMJ 2015;350:h1295

March 5, 2105.

From the world’s most prestigious medical journal, the New England Journal of Medicine, a landmark study showing improved air quality pays off with improved lung function and actual growth of lung capacity in children. This not only improves cardiovascular capability, but is a key factor in avoiding adult onset of lung and heart disease and increasing life expectancy, which is highly correlated with lung function.

March 5, 2015. Another study showing kids exposed to more traffic pollution demonstrate intellectual impairment compared to their non-exposed peers. In this study, similar to other studies, the cognitive loss was over 4%.

Sunnier J, et al. Association between Traffic-Related Air Pollution in Schools and Cognitive Development in Primary School Children: A Prospective Cohort Study. PLOS medicine. Published: March 3, 2015DOI: 10.1371/journal.pmed.1001792

Feb. 28, 2015. Even a modest program of curtailing community wood smoke in the San Joaquin Valley resulted in a significant reduction in PM2.5, about 15%, and a similar reduction in hospitalization for ischemic heart disease. Salt Lake City would undoubtedly have an even greater benefit because the average winter temperature in Salt Lake is about ten degrees colder than the San Joaquin Valley, therefore more wood is being burned.

Feb. 16, 2015 Another recent study compared daily hospital admissions and death rates related to cardiovascular and pulmonary diseases among two cities in South America where one city’s pollution was predominantly from wood smoke and another was from mobile and typical point sources. Compared to the non-wood burning city, the city with primarily wood smoke experienced an increase of 47% for cardiorespiratory deaths, and an increase of 104% for respiratory hospital admissions for every 10 ug/m3 increase in PM10